Neurotransmitter systems of some brain regions of rats subjected to chronic morphine intoxication

2011 ◽  
Vol 5 (2) ◽  
pp. 175-179
Author(s):  
S. V. Lelevich ◽  
A. A. Novokshonov
Keyword(s):  
Brain Regions ◽  
Chronic Morphine ◽  
Neurotransmitter Systems ◽  
Chronic Morphine Intoxication

scholarly journals Neuromediator systems in some brain regions of rats subjected to morphine intoxication

2010 ◽  
Vol 56 (5) ◽  
pp. 562-569
Author(s):  
S.V. Lelevich ◽  
A.A. Novokshonov
Keyword(s):  
Brain Stem ◽  
Brain Tissue ◽  
Brain Regions ◽  
Cerebral Hemispheres ◽  
Serotonin Level ◽  
Chronic Morphine ◽  
Chronic Morphine Intoxication ◽  
System Functioning ◽  
Gaba Content ◽  
The Brain

The content of neuromediators and its metabolites in the cortex of cerebral hemispheres, in thalamus and brain stem was studied under chronic morphine intoxication (7-21 days). The morphine intake during 7-14 days was accompanied by changes of catecholamine system functioning, which was the most pronounced in the thalamus and the brain stem. These changes included increased secretion of dophamine and noradrenaline, their decrease in the brain tissue, and the increased content of their metabolites. The changes of serotonin and GABA content were less pronounced and included a decrease of serotonin level and the increase of the GABA content in different periods of narcotization.

Effect of chronic morphine treatment on the adrenaline biosynthesis in adrenals and brain regions of the rat

1988 ◽  
Vol 37 (4) ◽  
pp. 749-752 ◽  
Author(s):  
Agnes Simonyi ◽  
Bela Kanyicska ◽  
Tibor Szentendrei ◽  
Marton I.K. Fekete
Keyword(s):  
Brain Regions ◽  
Morphine Treatment ◽  
Chronic Morphine ◽  
Chronic Morphine Treatment

scholarly journals Mu opioid receptor and orexin/hypocretin mRNA levels in the lateral hypothalamus and striatum are enhanced by morphine withdrawal

2006 ◽  
Vol 191 (1) ◽  
pp. 137-145 ◽  
Author(s):  
Yan Zhou ◽  
Jacob Bendor ◽  
Lauren Hofmann ◽  
Matthew Randesi ◽  
Ann Ho ◽  
...  
Keyword(s):  
Opioid Receptor ◽  
Lateral Hypothalamus ◽  
Brain Regions ◽  
Mu Opioid Receptor ◽  
Morphine Withdrawal ◽  
Mrna Levels ◽  
Chronic Morphine ◽  
Mu Opioid ◽  
Morphine Administration ◽  
Related Stress

In this study, we investigated the effects of acute morphine administration, chronic intermittent escalating-dose morphine administration and spontaneous withdrawal from chronic morphine on mRNA levels of mu opioid receptor (MOP-r), and the opioid peptides pro-opiomelanocortin (POMC) and preprodynorphin (ppDyn) in several key brain regions of the rat, associated with drug reward and motivated behaviors: lateral hypothalamus (lat.hyp), nucleus accumbens (NAc) core, amygdala, and caudate–putamen (CPu). There was no effect on MOP-r mRNA levels in these brain regions 30 min after either a single injection of morphine (10 mg/kg, i.p.) or chronic intermittent escalating-dose morphine (from 7.5 mg/kg per day on day 1 up to 120 mg/kg per day on day 10). Activation of the stress-responsive hypothalamic–pituitary–adrenal axis by 12 h withdrawal from chronic morphine was confirmed; both POMC mRNA levels in the anterior pituitary and plasma adrenocorticotropic hormone levels were significantly elevated. Under this withdrawal-related stress condition, there was an increase in MOP-r mRNA levels in the lat.hyp, NAc core, and CPu. Recent studies have demonstrated a novel role for the lat.hyp orexin (or hypocretin) activation in both drug-related positive rewarding, and withdrawal effects. Around 50% of lat.hyp orexin neurons express MOP-r. Therefore, we also examined the levels of lat.hyp orexin mRNA, and found them increased in morphine withdrawal, whereas there was no change in levels of the lat.hyp ppDyn mRNA, a gene coexpressed with the lat.hyp orexin. Our results show that there is an increase in MOP-r gene expression in a region-specific manner during morphine withdrawal, and support the hypothesis that increased lat.hyp orexin activity plays a role in morphine-withdrawal-related behaviors.

scholarly journals Evaluation of Schizophrenic Activity in Experimental Animals

2021 ◽  
Vol 9 (12) ◽  
pp. 1269-1278
Author(s):  
Mr. Katkure Pawan Mahadev
Keyword(s):  
Animal Models ◽  
Clinical Presentation ◽  
Clinical Symptoms ◽  
Critical Evaluation ◽  
Brain Regions ◽  
Future Research ◽  
Neurotransmitter Systems ◽  
Experimental Animals ◽  
Animal Modeling

Abstract: The use of current research into schizophrenia has remained highly fragmented, much like the clinical presentation of the disease itself. Differing theories as to the cause and progression of schizophrenia, as well as the heterogeneity of clinical symptoms, have made it difficult to develop a coherent framework suitable for animal modeling. However, a number of limited animal models have been developed to explore various causative theories and to test specific mechanistic hypotheses. Historically, these models have been based on the manipulation of neurotransmitter systems believed to be involved in schizophrenia. In recent years, the emphasis has shifted to targeting relevant brain regions in an attempt to explore potential etiologic hypotheses. The specific animal models developed within these frameworks are described in this review. Emphasis is placed on the critical evaluation of currently available models because these models help to shape the direction of future research.

Expression and colocalization of NMDA receptor and FosB/ΔFosB in sensitive brain regions in rats after chronic morphine exposure

2016 ◽  
Vol 614 ◽  
pp. 70-76 ◽  
Author(s):  
Qiang Zhang ◽  
Qi Liu ◽  
Tongzhou Li ◽  
You Liu ◽  
Lei Wang ◽  
...  
Keyword(s):  
Nmda Receptor ◽  
Brain Regions ◽  
Chronic Morphine

Antibodies to morphine as indicators of chronic morphine intoxication and impaired immune reactivity

1996 ◽  
Vol 1 (4) ◽  
pp. 437-445 ◽  
Author(s):  
NATALIA GAMALEYA ◽  
SERGEI TRONNIKOV ◽  
LUDMILA ULYANOVA ◽  
SVETLANA KLIMOVA ◽  
IRINA DMITRIEVA
Keyword(s):  
Immune Reactivity ◽  
Chronic Morphine ◽  
Antibodies To Morphine ◽  
Chronic Morphine Intoxication

Nicotine during pregnancy: changes induced in neurotransmission, which could heighten proclivity to addict and induce maladaptive control of attention

2014 ◽  
Vol 6 (3) ◽  
pp. 169-181 ◽  
Author(s):  
K. A. Kohlmeier
Keyword(s):  
Neuronal Development ◽  
Drugs Of Abuse ◽  
Brain Regions ◽  
Prenatally Exposed ◽  
Laterodorsal Tegmental Nucleus ◽  
Neurotransmitter Systems ◽  
Tegmental Nucleus ◽  
Gestational Exposure ◽  
Transdermal Nicotine ◽  
Targeted Treatments

Prenatal exposure to nicotine, occurring either via maternal smoking or via use of transdermal nicotine patches to facilitate cigarette abstinence by pregnant women, is associated with ∼13% of pregnancies worldwide. Nicotine exposure during gestation has been correlated with several negative physiological and psychosocial outcomes, including heightened risk for aberrant behaviors involving alterations in processing of attention as well as an enhanced liability for development of drug dependency. Nicotine is a terotogen, altering neuronal development of various neurotransmitter systems, and it is likely these alterations participate in postnatal deficits in attention control and facilitate development of drug addiction. This review discusses the alterations in neuronal development within the brain’s major neurotransmitter systems, with special emphasis placed on alterations within the laterodorsal tegmental nucleus, in light of the role this cholinergic nucleus plays in attention and addiction. Changes induced within this nucleus by gestational exposure to nicotine, in combination with changes induced in other brain regions, are likely to contribute to the transgenerational burden imposed by nicotine. Although neuroplastic changes induced by nicotine are not likely to act in isolation, and are expected to interact with epigenetic changes induced by preconception exposure to drugs of abuse, unraveling these changes within the developing brain will facilitate eventual development of targeted treatments for the unique vulnerability for arousal disorders and development of addiction within the population of individuals who have been prenatally exposed to nicotine.

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